2 Hypertension June 2018 observed in individuals with the maximum sodium excretion combined with the lowest potassium excretion. 8 Similarly, a cluster-randomized controlled trial, in which participants increased potassium consumption and reduced sodium consumption, showed reduced cardiovascular mortality among those assigned to the higher potassium group. 17 Animal studies using established hypertensive models further provide critical evidence of potassium in the control of BP. In the 1950s, Meneely et al18, 19 found that potassium administration modulated BP and significantly enhanced survival of rats fed high-NaCl diet. In another classical work, Dahl et al20 found that the life expectancy of the rats, although shortened by high doses of sodium, increased back toward untreated values by concurrent supplementation with potassium. After establishing that the dietary Na/K ratio is crucial for long-term survival, Dahl et al went on to test the effect of different dietary Na/K ratios in hypertension-prone rats. All tested diets had high NaCl content (4.50%) but differed in KC1 concentration. It was concluded that the dietary Na/K molar ratio could be an important determinant of the severity, or even development, of salt-induced hypertension. 20 Tobian et al further uncovered the benefits of potassium supplementation during the development of hypertension and renal disease. Thus, the addition of 1.36% K+ to the diet reduced renal lesions (by 50% in the renal cortex, by 30% in the outer medulla, and by 44% in the inner medulla) in high salt-fed Dahl SS (salt sensitive) rats. 21 The added potassium also decreased BP moderately in SHR (spontaneously hypertensive) rats and modestly in Dahl SS rats. Importantly, the high-K+ diet had a striking effect on mortality in both models. After 17 weeks on a 4% NaCl diet with no added K+, 20 of 24 SHR rats had died. On the contrary, 49 of 50 rats on the same diet plus 1.36% K+ were still alive. This resulted in a 98% reduction in mortality rate (Figure 1A). 22 Similarly, after 9 weeks on the high-salt (8% NaCl) diet with no K+ supplement, 18 of 33 Dahl SS rats had died, whereas only 2 of 45 rats with 1.36% K+ supplementation had perished (overall, 93% reduction in mortality rate; Figure 1B). 22 These changes in survival rate occurred independently from BP, and it is likely that the majority of these deaths was because of stroke. Furthermore, it was reported that the level of dietary potassium has a marked influence on NaCl sensitivity in SHR rats, which are considered NaCl resistant. 23 Another chronic study of Dahl SS rats fed 1% NaCl with increasing dietary KCl revealed that after 8 months, Dahl SS rats fed 1% NaCl supplemented with 0.7% KCl had significantly increased mean arterial pressure, plasma volume, cardiac output, and renal and cerebral vascular resistance compared with Dahl salt-resistant rats receiving the same diet. All these parameters were significantly reduced, when dietary K+ supplement was increased to 2.6%. 24 Providing further evidence supporting the importance of dietary potassium in renal disease and hypertension, it has been reported that potassium depletion and hypokalemia induce renal injury, salt sensitivity, and hypertension in rats. 25, 26 For example, Sprague Dawley rats have significant growth retardation, increased renin–angiotensin system activity, tubulointerstitial injury, macrophage infiltration, and early fibrosis when fed a potassium-deficient (< 0.05% K+) diet. Furthermore, these rats had elevated BP and increased salt sensitivity. 25 In summary, dietary supplementation of potassium can lower BP in human and animal models, especially if they are prone to have salt …